The biological mechanisms that underlie fetal alcohol spectrum disorder (FASD) are complex and poorly understood. This thesis aims to investigate potential underlying mechanisms of FASD by using zebrafish as a model organism. The research question asked is how does embryonic alcohol exposure alter brain function and behavior in different zebrafish strains? My first experiment explored the influence of environmental factors salinity and olfactory cues on zebrafish behavior. This was conducted to reduce experimental error variation and create more sensitive behavioral paradigms. My second experiment focused on characterizing the development of shoaling behavior and correlated neurochemicals in the absence of embryonic alcohol in order to establish baseline behavior. Next, I examined the effect of embryonic alcohol exposure on neurochemicals dopamine, serotonin and their metabolites and found embryonic alcohol exposure to disrupt the dopaminergic and serotonergic systems in the developing fish; as well I discovered these effects to be strain- dependent. I found that the specific development time point, concentration and short duration of alcohol exposure used in my experiments do not alter amino acid neurotransmitters glutamate, glycine, aspartate, taurine and GABA. Lastly, I have investigated apoptosis and have adapted the labeling TUNEL assay, for zebrafish. I found that mild alcohol exposure during development results in an increase in apoptosis and that these early responses result in long-lasting changes in neuronal markers and number of cells in specific brain areas. I included results on different zebrafish strains in some of my studies. Strain differences will facilitate the discovery of molecular mechanisms underlying changes in alcohol-related genes and will also allow researchers to choose the more appropriate strain for drug or mutation screening all of which will facilitate a better understanding of FASD.